Aflatoxicosis in Poultry

ISSN 2349-7823
International Journal of Recent Research in Life Sciences (IJRRLS)
Vol. 3, Issue 3, pp: (15-19), Month: July - September 2016, Available at: www.paperpublications.org
Page | 15
Paper Publications
Aflatoxicosis in Poultry
Sakshi Tiwari1
, Vikash Sharma2
, Amrender Nath Tiwari3
, Amit Shukla4
1, 2
Department of Veterinary Pathology, LUVAS, Hisar, India
3
Vet Serv Diagnostics, New Delhi
4
Department of Veterinary physiology and Biochemistry, Arawali Veterinary college, Sikar, Rajsthan,India
Abstract: Aflatoxicosis is among the major cause of economic losses in poultry production. Aflatoxins are a group
of hepatotoxic compounds produced by the fungus of Aspergillus sps. when growing on feedstuffs. Aflatoxins are
hepatotoxic, mutagenic and carcinogenic fungal toxin which is capable of producing diseases in farm animals as
well as poultry. There are four primary aflatoxins: aflatoxin B1 (AFB1), aflatoxin B2 (AFB2), aflatoxin G1 (AFG1)
and aflatoxin G2 (AFG2). Among these AFB1 is the most toxic aflatoxin. Aflatoxicosis in poultry is characterized
by decreased growth rate, poor feed conversion, immunosuppression, passage of undigested food in the dropping,
anemia, decrease egg production in layers quantitatively and qualitatively, decrease hatchability, embryonic
mortality, reduced fertility due to decrease testicular weight, decrease semen volume and sometimes there may be
lamness, ataxia, convulsions & death. In humans being acute aﬂatoxicosis is manifested by vomiting, abdominal
pain, pulmonary edema, coma, convulsions, and death with cerebral edema and fatty involvement of the liver,
kidney and heart.
Keywords: Aflatoxin, Poultry, Hepatotoxic.
1. INTRODUCTION
Mycotoxins are ubiquitous in nature and produced by several fungi. Many species of fungi like Aspergillus, Fusarium,
Penicillium, Claviceps, and Alternaria etc particularly produces these mycotoxins. Mycotoxins are the secondary
metabolites of fungi. Over 400 known mycotoxins have been identified with a potential 30,000 different metabolites.
Most common mycotoxicosis affecting commercial poultry are Aflatoxicosis and ochratoxicosis (Pattison et al., 2008).
Aflatoxin is hepatotoxic, mutagenic and carcinogenic fungal toxin which is capable of producing diseases in farm animals
as well as poultry and is known to be produced by specific moulds in feed commodities (Bennet and Klich, 2003).
Aspergillus species produce most potent fungal toxin causing aflatoxicoses that have harmful effects on living beings.
Aflatoxins belong to a heterologous group of fungal secondary metabolites called mycotoxins that adversely affect human
and animal health. Aflatoxins are most commonly produced by strains of Aspergillus flavus, A. parasiticus, and A.
nominus, although many other Aspergilli have aflatoxin producing capabilities. Of the over 180 species of Aspergillus,
only a few are aflatoxigenic. Aflatoxins are named according to their blue or green fluorescence under UV light, there are
four primary aflatoxins: aflatoxin B1 (AFB1), aflatoxin B2 (AFB2), aflatoxin G1 (AFG1) and aflatoxin G2 (AFG2)
(Yiannikouris and Jouany, 2002). AFB1 is the most toxic and is classified as human carcinogen (Talebi et al., 2011).
Molecular structures of the four primary aflatoxins

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Paper Publications
In humans, acute aﬂatoxicosis there is vomiting, abdominal pain, pulmonary edema, coma, convulsions, and death with
cerebral edema and fatty involvement of the liver, kidney and heart (Strosnider et al., 2006).
Sources:
Poultry birds become exposed to AFB1 and other aflatoxins by consuming contaminated feed. Corn, cottonseed, peanuts,
sorghum and other foods (figs,tree nuts and spices) are at especially high risk. Warm and humid conditions during
maturation, harvest, transport or storage, promote Aspergillus growth and aflatoxin production. Aflatoxins can also be
transfered to milk, meat and eggs of livestock and poultry fed the toxins. Therefore, AFB1 is a human food safety risk in
both plant and animal products.
Sensitivity:
Ducks > Turkeys > Japanese quail > Chickens (Lozano and Diaz,2006; Rawal and Kim, 2010)
AFB1 Metabolism:
AFB1 require bioactivation for to be toxic and bioactivation predominantly occurs in liver (Bedard and Massey, 2006 and
Rawal and Kim, 2010). AFB1 is absorbed in the small intestine and majority of the toxin is metabolized in the liver. In the
liver AFB1 is converted by hepatic cytochromes P450 enzymes into the reactive and electrophilic AFB1-8,9- exo-
epoxide (AFBO) (Bedard and Massey, 2006; Eaton and Gallagher, 1994; Rawal and Kim, 2010; Klein et. al, 2000). An
endo stereoisomer of AFBO epoxide can also be produced, but is less toxic and is not relevant to AFB1 toxicity (Bedard
and Massey, 2006; Eaton and Gallagher, 1994). AFBO is a highly unstable intermediate and quickly reacts to form
adducts with DNA, RNA and proteins, responsible for AFB1 toxicity (Bedard and Massey, 2006; Eaton and Gallagher,
1994). AFBO is primarily detoxified by glutathione S-transferase (GST) enzymes that add glutathione (GSH) to form an
8,9-dihydro-8-(S-glutathionyl)-9-hydroxy-AFB1 (AFB1-SG) adduct.( Rawal and Kim, 2010; Eaton and Gallagher, 1994;
Klein et. al, 2000). Other metabolites of AFB1 are aflatoxicol, aflatoxin M1, aflatoxin P1 and aflatoxin Q1.
Clinical signs:
Clinical signs of aflatoxicosis in poultry envolves decreased growth rate, poor feed conversion, immunosuppression,
vaccination failure, decrease resistance to infectious disease, passage of undigested food in the dropping, anemia, decrease
egg production in layers quantitatively and qualitatively, decrease hatchability, embryonic mortality, reduced fertility due
to decrease testicular weight, decrease semen volume (sperm counts), and sometimes there may be lamness, ataxia,
convulsions & death.
Symptoms depend on the type of toxin, amount, duration of the exposure, age, health status and synergistic effects of
genetics, dietary status, and interactions with other toxic insults (Bennett and Klich, 2003).
Post mortem findings:
Liver becomes swollen, friable, pale or yellow due to precipitation of fat and hyperplasia of bile ducts epithelium,
inflammation of these ducts , gallbladder enlarged and in the late stage fibrosis of the liver may occur. Enlargement of the
kidneys, spleen and pancreas. Atrophy of bursa of Fabricius, thymus and testes. Hemorrhages present under the skin, on
muscles and on the internal organs due to fragility of blood vessels (Biro et al., 2002). In chronic stage there is ascites and
hydropericardium.
2. HISTOPATHOLOGY
Liver reaveled vacuolation of hepatic cells and bile duct proliferation. Metabolic alterations caused by aflatoxins in
chickens result in elevated lipid levels, disruptions in hepatic protein synthesis, which result in several blood coagulation
disorders, immunosuppression and decreased plasma amino acid concentrations (Sumit et al., 2010). Kidneys revealed
thickened basement membrane in the glomeruli and associated hyaline droplets in the renal tubules. It is not known if the
glomerulus is damaged by toxins or by a leakage of unusual protein from a severely damaged liver. Liver lesions in
chicken are characterized by retrogressive and regenerative parenchymal changes. (Herenda and Franco, 1996). R.E. cell
hyperplasia along with depletion of lymphocyte observed in spleen. Bursa of Fabricus revealed degeneration and
depletion of lymphoid cells in bursal follicle.
3. DIAGNOSIS
Diagnosis is based on history, clinical signs, gross and microscopic lesions. By examination of grains or feeds externally
showing change in colour or growth of fungi. Definite diagnosis depends on identification of toxin.

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Traditional methods: Bioassays using ducklings, chicken embryos and brine shrimp larvae were used for toxicity testing
of feed ingredients (Watson and Lindsay, 1982; Celik et al., 2000).
Now a days detection largely depends on chromatographic techniques using sophisticated equipments. HPLC using
fluorescence detection become the most accepted method for the determination of aflatoxins (Blesa et al., 2005). Rapid
immunochemical screening methods like enzyme-linked immunosorbent assay (ELISA) and immunoaffinity column
assay (ICA) have been developed and are commercially available (Schiefer, 1990). Rapid minicolumn method for
aflatoxin detection in agricultural products (Arim et al., 1999). El-Nagerabi and Elshafie (2001) developed a test known
as the Bright greenish-yellow fluorescence (BGYF) test. Feed samples are inspected under UV light for a characteristic
bright greenish yellow fluorescence in damaged kernels. ELISA has been routinely used for detection of aflatoxin B1 in
cereals and animal tissues (Dutta and Das, 2001; Gathumbi et al., 2003; Lee et al., 2004). An antibody-colloidal gold
probe conjugate has been developed recently for rapid and specific detection of AFB1. Mass spectroscopy(MS) in
combination with liquid chromatography is becoming popular for identification of aflatoxins (Sulyok et al.,2006;
Cavaliere et al., 2007).
Recent and advanced techniques
 Biosensors: Biosensor assay works on the surface plasmon resonance (SPR) (Zheng and Binder, 2005; Logrieco et
al.,2005).
 MicroSERS is a new biochip technology that uses surface-enhanced Raman scattering (SERS) microscopy for label-
free transduction and detection of aflatoxins (Grow et al., 2003).
 Polymerase chain reaction (PCR): Primers for aflatoxin regulatory (afl R), o-methyltransferase (omt) and
oxidoreductase (ord) genes are used.
Strategies to Reduce AFB1 Toxicity:
 Use of preservatives and anti-fungal agents, such as propionic acid.
 Mould inhibitors like hydroxyquinoline effective in reducing aflatoxin formation (Rao, 1995).
 Chemical Detoxification: Ammonium hydroxide, calcium hydroxide, sodium hydroxide and sodium hypochlorite
reduce AFB1 concentrations through hydrolysis.
 Probiotics: Many Gram-positive bacteria, including Streptococcus, Enterococcus, Lactococcus, and Berevibacillus,
can bind AFB1. Interactions between AFB1 and Lactobacillus rhamnosus GG L.rhamnosus LC-705 or mixtures of
these strains have been shown to be especially effective.
 Selection for Resistance: Selection for AFB1 resistant lines of chicken and quail has been investigated.
4. PREVENTION
For prevention of aflatoxicosis shipments falling outside acceptable levels should be rejected. Antifungals as organic
acids, copper sulphate, gentin violet must be added routinely to the feeds to prevent fungal growth in storage feeds.Ozone
treatment of grain can be used. Feed must be stored in well ventilated place, and walls to avoid excess moisture. Feed
should be prepared fresh as fresh (store time must not exceed than 14 days). Litter must stored in well ventilated places
and in poultry house must preserved it dry. We should use the practice of regular inspection of feed and cleaning and
disinfections of grain mills, feeding troughs with formalin 2-3 % or copper sulphate. Pelleted feed should be preffered
because during their manufacturing process cause destruction of fungal spores.
5. CONCLUSIONS
Aflatoxins are considered as primary cause of abnormal health status and productive performances in birds. Because of
increased susceptibility to infections and drastic reduction in production potential aflatoxins causes a significant loss to
poultry industry. Aflatoxins are of much concern to humans also as it is present as residues in milk, meat, eggs and other
animal products. Detoxifying agents and toxin binders have to be used in order to make sure that the animals are receiving
safer feed materials. Future gene expression analyzes can provide insight into the mechanisms of aflatoxicosis and
methods to reduce its effects. Education and awareness of farmers about aflatoxicosis is important for dealing with this
problem. Organizations at National and International level are to constantly monitor the risk aflatoxins poses to animal
health and need to draft legal limits for their effective control and prevention.

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REFERENCES
[1] Arim R H, Aguinaldo A R, Tanaka T and Yoshizawa T. (1999). Optimization and validation of a minicolumn
method for determining aflatoxins in copra meal. J. Assoc. Off. Anal. Chem.82(4): 877-878.
[2] Bedard L L and Massey T E. (2006). Aflatoxin B1-induced DNA damage and its repair. Cancer Lett. 241:174–
183.
[3] Bennett J W and Klich M. (2003). Mycotoxins. Clin. Microbiol. Rev. 16(3): 497-516.
[4] Biró K, Solti L, Barna-Vetró I, Bagó G, Glávits R, Szabó E and Fink-Gremmels J (2002). Tissue distribution of
ochratoxin A as determined by HPLC and ELISA and histopathological effects in chickens, Avian Pathology. 31:2,
141-148.
[5] Blesa J, Soriano J M, Molto J C and Manes J. (2005). Analysis of aflatoxins in peeled peanuts by liquid
chromatography and fluorescence detection. Bull. Environ. Contam. Toxicol. 75(1,2): 115-120.
[6] Cavaliere C, Foglia P, Guarino C, Nazzari M, Samperi R and Lagana A. (2007). A sensitive confirmatory method
for aflatoxins in maize based on liquid chromatography/electrospray ionization tandem mass spectrometry. Rapid
Commun. Mass Spectrom. 21(4): 550-556.
[7] Celik I, Oguz H, Demet O, Boydak M, Donmez HH, Sur E and Nizamlioglu F. (2000). Embryotoxicity assay of
aflatoxin produced by Aspergillus parasiticus NRRL 2999. Br. Poult. Sci. 41(4): 401-409.
[8] Dutta T K and Das P. (2001). Isolation of aflatoxigenic strains of Aspergillus and detection of aflatoxin B1 from
feeds in India. Mycopathologia. 151(1 & 2): 29-33.
[9] Eaton D L and Gallagher E P. (1994). Mechanisms of aflatoxin carcinogenesis. Annu. Rev. Pharmacol. Toxicol.
34: 135–172.
[10] El-Nagerabi S A and Elshafie A E. (2001). Incidence of seed-borne fungi and aflatoxins in Sudanese lentil seeds.
Mycopathologia.149(3):151-156.
[11] Gathumbi J K, Usleber E, Ngatia T A, Kangethe E K and Martlbauer E. (2003). Application of immunoaffinity
chromatography and enzyme immunoassay in rapid detection of aflatoxin B1 in chicken liver tissues. Poult. Sci.
82(4): 585-590.
[12] Grow A E, Wood L L, Claycomb J L and Thompson P A. (2003). New biochip technology for label-free detection
of pathogens and their toxins. J. Microbiol. Methods. 53 (2): 221-233.
[13] Herenda D.C. and Don A. (1996).Franco-Poultry Diseases and Meat Hygiene.1st
edn. Iowa State, University Press,
Ames.
[14] Klein P J, Buckner R, Kelly J and Coulombe R A (2000) Jr. Biochemical basis for the extreme sensitivity of
turkeys to aflatoxin B1. Toxicol. Appl. Pharmacol. 165: 45–52.
[15] Lee N A, Wang S, Allan R D and Kennedy I R. (2004). A rapid aflatoxin B1 ELISA: development and validation
with reduced matrix effects for peanuts, corn, pistachio, and Soybeans. J. Agric. Food Chem. 52(10): 2746-2755.
[16] Logrieco A, Arrigan D W, Brengel-Pesce K, Siciliano P and Tothill I. (2005). DNA arrays, electronic noses and
tongues, biosensors and receptors for rapid detection of toxigenic fungi and mycotoxins: A review. Food Addit.
Contam. 22(4):335-344.
[17] Lozano, M C and Diaz, G J. (2006). Microsomal and cytosolic biotransformation of aflatoxin B1 in four poultry
species. Br. Poult. Sci. 47: 734–741.
[18] Pattison M, McMullin P, Bradbury J, Alexander D (2008).Poultry Diseases.6th
edn. Chapter 38, pages 435-442.
[19] Rao, J R, Sharma, N N and Johri, T S (1995). Influence of dietary aflatoxin on Eimeria uzura infection in Japanese
quail (Coturnix coturnix japonica). Vet. Parasitol. 56: 17–22.

ISSN 2349-7823
Page | 19
Paper Publications
[20] Rawal S, Kim J E and Coulombe R. (2010). Aflatoxin B1 in poultry: Toxicology, metabolism and prevention. Res.
Vet. Sci. 89: 325–331.
[21] Schiefer H B. (1990). Mycotoxicosis of domestic animals and their diagnosis. Can. J. Physiol. Pharmacol. 68:
987-990.
[22] Strosnider H, Azziz-Baumgartner E, Banziger M, Bhat R V, Breiman R, Brune M N, DeCock K, Dilley A,
Groopman J, Hell K, Henry S H, Jeffers D, Jolly C, Jolly P, Kibata G N, Lewis L, Liu X, Luber G, McCoy L,
Mensah P, Miraglia M, Misore A, Njapau H, Ong C N, Onsongo M T, Page S W, Park D, Patel M, Phillips T,
Pineiro M, Pronczuk J, Rogers H S, Rubin C, Sabino M, Schaafsma A, Shephard G, Stroka J, Wild C, Williams J
T and Wilson D. (2006). Workgroup report: public health strategies for reducing aﬂatoxin exposure in developing
countries. Environmental Health Perspectives 114:1898–1903.
[23] Sulyok M, Berthiller F, Krska R and Schuhmacher R. (2006). Development and validation of a liquid
chromatography/tandem mass spectrometric method for the determination of 39 mycotoxins in wheat and maize.
Rapid Commun. Mass Spectr. 20(18): 2649-2659.
[24] Sumit R, Kim E J and Coulombe R. (2010). Aflatoxin B1 in poultry: Toxicology, metabolism and prevention.
Research in Veterinary Science. 89: 325–331.
[25] Talebi E, Khademi M and Rastad A (2011). An Over Review on Effect of Aflatoxin in Animal Husbandry. Asian
J. Exp. Biol. Sci. Vol. 2(3): 754 – 757.
[26] Watson D H and Lindsay D G. (1982). A critical review of biological methods for the detection of fungal toxins in
foods and feedstuffs, J. Sci. Food Agri. 33: 59–67.
[27] Yiannikouris A and Jouany J P. (2002). Mycotoxins in feeds and their fate in animals: A review. Anim. Res. 51:
81-99.
[28] Zheng M Z and Binder J. (2005). Rapid testing of total aflatoxin in agricultural raw materials. Poult. Planner. 7(5):
12-14.

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